Pathology chapters
Oedema and shock
Why fluid leaks out of vessels (Starling forces, lymph block, salt retention), oedema in heart failure, ascites, hydrothorax and anasarca, and the main types of shock, their compensation and the stages from reversible to irreversible.
- Oedema is excess fluid in the interstitial tissue or body cavities; causes: raised hydrostatic pressure (heart failure, DVT), low plasma oncotic pressure (nephrotic syndrome, cirrhosis, malnutrition), lymphatic obstruction (filariasis, surgery), sodium retention and inflammation.
- Ascites (peritoneal cavity), hydrothorax (pleural cavity) and anasarca (severe generalised oedema) are its forms; heart failure causes oedema through high venous pressure plus renin-angiotensin-aldosterone-driven salt and water retention.
- Shock is systemic hypoperfusion from low cardiac output or low effective blood volume: hypovolaemic, cardiogenic, septic (the commonest cause of death in ICUs), neurogenic and anaphylactic; it passes from non-progressive (compensated) to progressive to irreversible.
On this page
Body water in brief
About 60% of body weight is water: two-thirds inside cells and one-third outside (interstitial fluid and plasma). Fluid moves between plasma and interstitium across capillary walls according to Starling forces.
Starling forces
- Hydrostatic pressure in the capillary pushes fluid out.
- Plasma oncotic (colloid osmotic) pressure, mainly from albumin, pulls fluid in.
- At the arterial end, outward pressure wins: fluid leaves.
- At the venous end, oncotic pressure wins: most fluid returns.
- Lymphatics return the small excess to the blood.
Net filtration pressure = (Pc − Pi) − (πc − πi)
Pc = capillary hydrostatic, Pi = interstitial hydrostatic, πc = plasma oncotic, πi = interstitial oncotic (mmHg)
Arterial end: Pc 35, Pi 0, πc 25, πi 1
Net = (35 − 0) − (25 − 1) = 35 − 24 = +11 → fluid moves OUT
Venous end: Pc 15, Pi 0, πc 25, πi 1
Net = (15 − 0) − (25 − 1) = 15 − 24 = −9 → fluid moves IN
Heart failure raises venous Pc to 30:
Net = (30 − 0) − (25 − 1) = +6 → fluid now leaves at the venous end too → oedema
Nephrotic syndrome drops πc to 15 (albumin lost in urine):
Venous end Net = (15 − 0) − (15 − 1) = +1 → reabsorption fails → oedema
These values are teaching figures to show the direction of movement; real values differ between tissues.
Oedema
Oedema is an abnormal build-up of fluid in the interstitial tissue or body cavities.
| Mechanism | Causes |
|---|---|
| Raised hydrostatic pressure | Congestive heart failure, deep vein thrombosis, constrictive pericarditis, portal hypertension (cirrhosis), venous obstruction |
| Reduced plasma oncotic pressure (low albumin) | Nephrotic syndrome (protein lost), cirrhosis (protein not made), malnutrition (kwashiorkor), protein-losing enteropathy |
| Lymphatic obstruction (lymphoedema) | Filariasis (elephantiasis of legs and scrotum), removal or radiation of axillary nodes (breast cancer), tumour spread; in breast cancer, blocked skin lymphatics give peau d'orange |
| Sodium and water retention | Renal failure, acute glomerulonephritis, heart failure (renin-angiotensin-aldosterone) |
| Inflammation (increased permeability) | Acute inflammation, burns, allergy (angioedema) |
Only inflammatory oedema is an exudate (protein-rich); all the other types produce a transudate (low protein).
Forms and sites
- Pitting oedema: finger pressure leaves a dent in the swollen skin; typical of dependent oedema in heart failure.
- Dependent oedema: in the lowest parts by gravity: ankles when up, sacrum when lying down (right heart failure).
- Periorbital oedema: loose tissue around the eyes; typical of renal oedema (nephrotic syndrome, glomerulonephritis), worst in the morning.
- Ascites: fluid in the peritoneal cavity (cirrhosis, heart failure, nephrotic syndrome, peritoneal tuberculosis or cancer).
- Hydrothorax: fluid in the pleural cavity (pleural effusion); hydropericardium: fluid in the pericardial sac.
- Anasarca: severe, generalised oedema of subcutaneous tissue with fluid in body cavities; seen in nephrotic syndrome, severe heart failure and hydrops fetalis.
Oedema in congestive cardiac failure
- The failing heart cannot pump blood forward → venous pressure rises → raised capillary hydrostatic pressure → oedema.
- Low cardiac output → less kidney perfusion → renin-angiotensin-aldosterone activation and ADH release → sodium and water retention → bigger blood volume → even higher venous pressure.
Left heart failure → pulmonary oedema; right heart failure → systemic (leg, sacral, liver) oedema and ascites.
Clinically important oedema
- Pulmonary oedema: commonest cause left ventricular failure; also ARDS, infections, renal failure. Lungs are 2–3 times their normal weight with frothy, sometimes blood-stained fluid; it impairs gas exchange and invites infection.
- Cerebral oedema: localised (abscess, tumour) or generalised (encephalitis, hypertensive crisis, trauma); can cause herniation of the brain through the foramen magnum and compress the brainstem, which can be fatal.
- Subcutaneous oedema: a pointer to heart or kidney disease; can delay wound healing and clearing of infection.
Shock
Shock is a state of systemic hypoperfusion of tissues caused by reduced cardiac output or reduced effective circulating blood volume. The result is hypotension, poor tissue oxygen delivery, cellular hypoxia and, if uncorrected, cell death and organ failure.
Types
| Type | Mechanism | Examples |
|---|---|---|
| Hypovolaemic | Loss of blood or plasma volume | Haemorrhage, severe diarrhoea and vomiting (cholera), burns, trauma |
| Cardiogenic | Pump failure | Myocardial infarction, arrhythmias, myocarditis, cardiac tamponade, massive pulmonary embolism (obstructive) |
| Septic | Vasodilation, leaky vessels and pooling from the host response to infection | Gram-negative infections (endotoxin, LPS) are classic; also Gram-positive and fungal infections |
| Neurogenic | Loss of vascular tone | Spinal cord injury, anaesthetic accidents |
| Vasovagal (reflex) | A sudden vagal reflex: bradycardia and vasodilation, briefly cutting brain perfusion | Fainting from pain, fear or the sight of blood; recovers quickly on lying flat |
| Anaphylactic | IgE-mediated vasodilation and leak | Drugs (penicillin), insect stings, foods |
Septic shock in more detail
Microbial products (for example LPS) activate macrophages, neutrophils and endothelium → TNF, IL-1 and other mediators →
- widespread vasodilation and increased permeability;
- endothelial activation and a procoagulant state → DIC;
- metabolic disturbance (insulin resistance, high then low blood sugar);
- immune suppression later in the course;
- multi-organ dysfunction (lungs, kidneys, liver, heart).
Early septic shock may show warm, flushed skin (vasodilation); hypovolaemic and cardiogenic shock show cool, pale, clammy skin (vasoconstriction).
Stages of shock
| Stage | What happens |
|---|---|
| 1. Non-progressive (compensated) | Reflexes keep blood pressure and vital organ perfusion: baroreceptor reflexes, catecholamine release (tachycardia, peripheral vasoconstriction), renin-angiotensin-aldosterone and ADH (retain salt and water). Blood is diverted to the brain and heart |
| 2. Progressive | Tissue hypoperfusion worsens; cells switch to anaerobic glycolysis → lactic acidosis; acidosis blunts vasoconstriction, so blood pools in the microcirculation; oliguria, confusion |
| 3. Irreversible | Severe cell and tissue injury; even if blood volume is restored, the patient cannot survive. Lysosomal enzyme leak, myocardial depression, acute tubular necrosis of the kidneys, ischaemic bowel lets gut bacteria into the blood |
Organ changes in shock
- Kidneys: acute tubular necrosis (oliguria).
- Lungs: diffuse alveolar damage (ARDS, "shock lung"), especially in septic shock.
- Brain: ischaemic encephalopathy.
- Heart: subendocardial haemorrhage and necrosis.
- Adrenals: lipid depletion; in meningococcal sepsis, bilateral adrenal haemorrhage (Waterhouse-Friderichsen syndrome).
- Gut: patchy mucosal haemorrhage and necrosis.
- Liver: fatty change, centrilobular necrosis.
Mean arterial pressure (MAP) = DBP + (SBP − DBP) ÷ 3
BP 90/60: MAP = 60 + (90 − 60) ÷ 3 = 60 + 10 = 70 mmHg
(Septic shock targets a MAP of at least 65 mmHg)
Shock index = heart rate ÷ systolic BP
HR 120, SBP 90: 120 ÷ 90 = 1.33
Normal is about 0.5–0.7; above about 1 suggests significant shock
Expect: Starling forces and how each disturbance causes oedema, nephrotic syndrome and low albumin, filariasis and lymphoedema, exudate vs transudate, the two mechanisms of oedema in heart failure, definitions of ascites, hydrothorax and anasarca, types of shock with examples, septic shock and LPS, compensatory mechanisms, the three stages of shock, and organ changes (ATN, ARDS, Waterhouse-Friderichsen).
Quick revision
- Oedema: high hydrostatic pressure, low oncotic pressure, lymph block, salt retention, inflammation.
- Only inflammatory oedema is an exudate.
- Heart failure oedema: high venous pressure plus RAAS salt and water retention.
- Ascites (peritoneum), hydrothorax (pleura), anasarca (generalised).
- Shock types: hypovolaemic, cardiogenic, septic, neurogenic, vasovagal, anaphylactic.
- Compensation: baroreceptors, catecholamines, RAAS, ADH.
- Stages: non-progressive → progressive (lactic acidosis) → irreversible.
- Organs: ATN, ARDS, adrenal haemorrhage in meningococcal sepsis.
Written by The House Job from standard pathology references (Robbins and Cotran Pathologic Basis of Disease is the book named in the UHS PGET syllabus).
FAQ
What is anasarca?
Severe generalised oedema of the subcutaneous tissues together with fluid in body cavities, seen for example in nephrotic syndrome.
Why does nephrotic syndrome cause oedema?
Albumin is lost in the urine, so plasma oncotic pressure falls and fluid stays in the tissues; salt retention adds to it.
What is the commonest cause of septic shock?
Classically Gram-negative bacterial infection, through endotoxin (LPS), though Gram-positive and fungal infections also cause it.
What are the compensatory mechanisms in shock?
Baroreceptor reflexes, catecholamine release (tachycardia and vasoconstriction), and the renin-angiotensin-aldosterone system and ADH, which retain salt and water.